治療標的としてのIL-23/IL-17連関
ヘルパーT（Th）細胞は周囲の環境に応じて各種のサブセットに分化することが知られている．2005年に報告・命名されたインターロイキン17（IL-17）産生性のTh17細胞サブセットは，炎症性疾患との関連が強く示唆されたことから精力的に解析が進められた．Th17細胞の分化条件，重要な転写因子やマウスとヒトとの異同などが次々に明らかになり，IL-17およびTh17細胞の活性化に重要とされるIL-23は創薬の有力な候補となった．実際にIL-23/IL-17連関を阻害する生物学的製剤が，特に皮膚の炎症性疾患である乾癬の治療薬として高い効果を示すことが報告され，実用化された．本稿では紆余曲折があったTh...
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| Published in | 日本臨床免疫学会会誌 Vol. 36; no. 4; pp. 203 - 208 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | Japanese |
| Published |
日本臨床免疫学会
2013
|
| Online Access | Get full text |
| ISSN | 0911-4300 1349-7413 |
| DOI | 10.2177/jsci.36.203 |
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| Abstract | ヘルパーT（Th）細胞は周囲の環境に応じて各種のサブセットに分化することが知られている．2005年に報告・命名されたインターロイキン17（IL-17）産生性のTh17細胞サブセットは，炎症性疾患との関連が強く示唆されたことから精力的に解析が進められた．Th17細胞の分化条件，重要な転写因子やマウスとヒトとの異同などが次々に明らかになり，IL-17およびTh17細胞の活性化に重要とされるIL-23は創薬の有力な候補となった．実際にIL-23/IL-17連関を阻害する生物学的製剤が，特に皮膚の炎症性疾患である乾癬の治療薬として高い効果を示すことが報告され，実用化された．本稿では紆余曲折があったTh17細胞の基礎研究と，生物学的製剤開発の現況について概説する． |
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| AbstractList | ヘルパーT（Th）細胞は周囲の環境に応じて各種のサブセットに分化することが知られている．2005年に報告・命名されたインターロイキン17（IL-17）産生性のTh17細胞サブセットは，炎症性疾患との関連が強く示唆されたことから精力的に解析が進められた．Th17細胞の分化条件，重要な転写因子やマウスとヒトとの異同などが次々に明らかになり，IL-17およびTh17細胞の活性化に重要とされるIL-23は創薬の有力な候補となった．実際にIL-23/IL-17連関を阻害する生物学的製剤が，特に皮膚の炎症性疾患である乾癬の治療薬として高い効果を示すことが報告され，実用化された．本稿では紆余曲折があったTh17細胞の基礎研究と，生物学的製剤開発の現況について概説する． 「抄録」ヘルパーT(Th)細胞は周囲の環境に応じて各種のサブセットに分化することが知られている. 2005年に報告・命名されたインターロイキン17(IL-17)産生性のTh17細胞サブセットは, 炎症性疾患との関連が強く示唆されたことから精力的に解析が進められた. Th17細胞の分化条件, 重要な転写因子やマウスとヒトとの異同などが次々に明らかになり, IL-17およびTh17細胞の活性化に重要とされるIL-23は創薬の有力な候補となった. 実際にIL-23/IL-17連関を阻害する生物学的製剤が, 特に皮膚の炎症性疾患である乾癬の治療薬として高い効果を示すことが報告され, 実用化された. 本稿では紆余曲折があったTh17細胞の基礎研究と, 生物学的製剤開発の現況について概説する. 「I. Th17細胞の発見」ヘルパーT(Th)細胞は細胞傷害性T(Tc)細胞と同様, 胸腺で分化する. その後末梢に移動し, Th1, Th2の2種類のサブセットに分化する1). |
| Author | 佐藤, 浩二郎 |
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| DOI | 10.2177/jsci.36.203 |
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| References | 43) Hueber, A.J., et al. : Mast cells express IL-17A in rheumatoid arthritis synovium. J Immunol 184 : 3336-3340, 2010. 14) Cua, D.J., et al. : Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature 421 : 744-748, 2003. 39) Papp, K.A., et al. : Brodalumab, an anti-interleukin-17-receptor antibody for psoriasis. N Engl J Med 366 : 1181-1189, 2012. 44) Suurmond, J., et al. : Mast cells are the main interleukin 17-positive cells in anticitrullinated protein antibody-positive and -negative rheumatoid arthritis and osteoarthritis synovium. Arthritis Res Ther 13 : R150, 2011. 45) Roark, C.L., et al. : gammadelta T cells : an important source of IL-17. Curr Opin Immunol 20 : 353-357, 2008. 27) Infante-Duarte, C., et al. : Microbial lipopeptides induce the production of IL-17 in Th cells. J Immunol 165 : 6107-6115, 2000. 49) Sandborn, W.J., et al. : Ustekinumab induction and maintenance therapy in refractory Crohn's disease. N Engl J Med 367 : 1519-1528, 2012. 41) Solt, L.A., et al. : Suppression of Th17 differentiation and autoimmunity by a synthetic ROR ligand. Nature 472 : 491-494, 2011. 42) Huh, J.R., et al. : Digoxin and its derivatives suppress Th17 cell differentiation by antagonizing RORgammat activity. Nature 472 : 486-490, 2011. 48) Lin, A.M., et al. : Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis. J Immunol 187 : 490-500, 2011. 10) Willenborg, D.O., et al. : IFN-gamma plays a critical down-regulatory role in the induction and effector phase of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis. J Immunol 157 : 3223-3227, 1996. 19) Acosta-Rodriguez, E.V., et al. : Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17-producing human T helper cells. Nat Immunol 8 : 942-949, 2007. 9) Voorthuis, J.A., et al. : Suppression of experimental allergic encephalomyelitis by intraventricular administration of interferon-gamma in Lewis rats. Clin Exp Immunol 81 : 183-188, 1990. 16) Kotake, S., et al. : IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J Clin Invest 103 : 1345-1352, 1999. 31) Nakae, S., et al. : Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J Immunol 171 : 6173-6177, 2003. 8) Krakowski, M., Owens, T. : Interferon-gamma confers resistance to experimental allergic encephalomyelitis. Eur J Immunol 26 : 1641-1646, 1996. 4) Vermeire, K., et al. : Accelerated collagen-induced arthritis in IFN-γ receptor-deficient mice. J Immunol 158 : 5507-5513, 1997. 32) Genovese, M.C., et al. : LY2439821, a humanized anti-interleukin-17 monoclonal antibody, in the treatment of patients with rheumatoid arthritis : A phase I randomized, double-blind, placebo-controlled, proof-of-concept study. Arthritis Rheum 62 : 929-939, 2010. 46) Cai, Y., et al. : Pivotal role of dermal IL-17-producing gammadelta T cells in skin inflammation. Immunity 35 : 596-610, 2011. 7) Ferber, I.A., et al. : Mice with a disrupted IFN-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J Immunol 156 : 5-7, 1996. 30) Huang, W., et al. : Requirement of interleukin-17A for systemic anti-Candida albicans host defense in mice. J Infect Dis 190 : 624-631, 2004. 15) Aggarwal, S., et al. : Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J Biol Chem 278 : 1910-1914, 2003. 28) Miossec, P., et al. : Interleukin-17 and type 17 helper T cells. N Engl J Med 361 : 888-898, 2009. 22) Volpe, E., et al. : A critical function for transforming growth factor-beta, interleukin 23 and proinflammatory cytokines in driving and modulating human T(H)-17 responses. Nat Immunol 9 : 650-657, 2008. 3) Manoury-Schwartz, B., et al. : High susceptibility to collagen-induced arthritis in mice lacking IFN-γ receptors. J Immunol 158 : 5501-5506, 1997. 24) Ivanov, I.I., et al. : The orphan nuclear receptor RORγt directs the differentiation program of proinflammatory IL-17+ T helper cells. Cell 126 : 1121-1133, 2006. 33) Griffiths, C.E., et al. : Comparison of ustekinumab and etanercept for moderate-to-severe psoriasis. N Engl J Med 362 : 118-128, 2010. 13) Oppmann, B., et al. : Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity 13 : 715-725, 2000. 50) Hirota, K., et al. : Fate mapping of IL-17-producing T cells in inflammatory responses. Nat Immunol 12 : 255-263, 2011. 20) Wilson, N.J., et al. : Development, cytokine profile and function of human interleukin 17-producing helper T cells. Nat Immunol 8 : 950-957, 2007. 21) Manel, N., et al. : The differentiation of human T(H)-17 cells requires transforming growth factor-beta and induction of the nuclear receptor RORgammat. Nat Immunol 9 : 641-649, 2008. 47) Pantelyushin, S., et al. : Rorgammat+ innate lymphocytes and gammadelta T cells initiate psoriasiform plaque formation in mice. J Clin Invest 122 : 2252-2256, 2012. 17) Bettelli, E., et al. : Reciprocal developmental pathways for the generation of pathogenic effector Th17 and regulatory T cells. Nature 441 : 235-238, 2006. 12) Park, H., et al. : A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nat Immunol 6 : 1133-1141, 2005. 18) Mangan, P.R., et al. : Transforming growth factor-β induces development of the Th17 lineage. Nature 441 : 231-234, 2006. 37) Chan, J.R., et al. : IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis. J Exp Med 203 : 2577-2587, 2006. 25) Kimura, A., et al. : Aryl hydrocarbon receptor regulates Stat1 activation and participates in the development of Th17 cells. Proc Natl Acad Sci USA 105 : 9721-9726, 2008. 35) Johnson-Huang, L.M., et al. : Effective narrow-band UVB radiation therapy suppresses the IL-23/IL-17 axis in normalized psoriasis plaques. J Invest Dermatol 130 : 2654-2663, 2010. 23) McGeachy, M.J., et al. : TGF-beta and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain T(H)-17 cell-mediated pathology. Nat Immunol 8 : 1390-1397, 2007. 1) Mosmann, T.R., et al. : Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins. J Immunol 136 : 2348-2357, 1986. 29) Ye, P., et al. : Requirement of interleukin 17 receptor signaling for lung CXC chemokine and granulocyte colony-stimulating factor expression, neutrophil recruitment, and host defense. J Exp Med 194 : 519-527, 2001. 38) Zheng, Y., et al. : Interleukin-22, a T(H)17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Nature 445 : 648-651, 2007. 5) Guedez, Y.B., et al. : Genetic ablation of interferon-gamma up-regulates interleukin-1beta expression and enables the elicitation of collagen-induced arthritis in a nonsusceptible mouse strain. Arthritis Rheum 44 : 2413-2424, 2001. 6) Billiau, A., et al. : Enhancement of experimental allergic encephalomyelitis in mice by antibodies against IFN-gamma. J Immunol 140 : 1506-1510, 1988. 36) Zaba, L.C., et al. : Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses. J Exp Med 204 : 3183-3194, 2007. 40) Leonardi, C., et al. : Anti-interleukin-17 monoclonal antibody ixekizumab in chronic plaque psoriasis. N Engl J Med 366 : 1190-1199, 2012. 51) Hirota, K., et al. : Plasticity of Th17 cells in Peyer's patches is responsible for the induction of T cell-dependent IgA responses. Nat Immunol 14 : 372-379, 2013. 2) Smolen, J.S., et al. : The role of T-lymphocytes and cytokines in rheumatoid arthritis. Scand J Rheumatol 25 : 1-4, 1996. 26) Veldhoen, M., et al. : The aryl hydrocarbon receptor links Th17-cell-mediated autoimmunity to environmental toxins. Nature 453 : 106-109, 2008. 11) Harrington, L.E., et al. : Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat Immunol 6 : 1123-1132, 2005. 34) Lee, E., et al. : Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris. J Exp Med 199 : 125-130, 2004. |
| References_xml | – reference: 19) Acosta-Rodriguez, E.V., et al. : Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17-producing human T helper cells. Nat Immunol 8 : 942-949, 2007. – reference: 11) Harrington, L.E., et al. : Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat Immunol 6 : 1123-1132, 2005. – reference: 44) Suurmond, J., et al. : Mast cells are the main interleukin 17-positive cells in anticitrullinated protein antibody-positive and -negative rheumatoid arthritis and osteoarthritis synovium. Arthritis Res Ther 13 : R150, 2011. – reference: 12) Park, H., et al. : A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nat Immunol 6 : 1133-1141, 2005. – reference: 50) Hirota, K., et al. : Fate mapping of IL-17-producing T cells in inflammatory responses. Nat Immunol 12 : 255-263, 2011. – reference: 45) Roark, C.L., et al. : gammadelta T cells : an important source of IL-17. Curr Opin Immunol 20 : 353-357, 2008. – reference: 4) Vermeire, K., et al. : Accelerated collagen-induced arthritis in IFN-γ receptor-deficient mice. J Immunol 158 : 5507-5513, 1997. – reference: 47) Pantelyushin, S., et al. : Rorgammat+ innate lymphocytes and gammadelta T cells initiate psoriasiform plaque formation in mice. J Clin Invest 122 : 2252-2256, 2012. – reference: 31) Nakae, S., et al. : Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J Immunol 171 : 6173-6177, 2003. – reference: 51) Hirota, K., et al. : Plasticity of Th17 cells in Peyer's patches is responsible for the induction of T cell-dependent IgA responses. Nat Immunol 14 : 372-379, 2013. – reference: 13) Oppmann, B., et al. : Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity 13 : 715-725, 2000. – reference: 9) Voorthuis, J.A., et al. : Suppression of experimental allergic encephalomyelitis by intraventricular administration of interferon-gamma in Lewis rats. Clin Exp Immunol 81 : 183-188, 1990. – reference: 46) Cai, Y., et al. : Pivotal role of dermal IL-17-producing gammadelta T cells in skin inflammation. Immunity 35 : 596-610, 2011. – reference: 29) Ye, P., et al. : Requirement of interleukin 17 receptor signaling for lung CXC chemokine and granulocyte colony-stimulating factor expression, neutrophil recruitment, and host defense. J Exp Med 194 : 519-527, 2001. – reference: 17) Bettelli, E., et al. : Reciprocal developmental pathways for the generation of pathogenic effector Th17 and regulatory T cells. Nature 441 : 235-238, 2006. – reference: 21) Manel, N., et al. : The differentiation of human T(H)-17 cells requires transforming growth factor-beta and induction of the nuclear receptor RORgammat. Nat Immunol 9 : 641-649, 2008. – reference: 34) Lee, E., et al. : Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris. J Exp Med 199 : 125-130, 2004. – reference: 6) Billiau, A., et al. : Enhancement of experimental allergic encephalomyelitis in mice by antibodies against IFN-gamma. J Immunol 140 : 1506-1510, 1988. – reference: 43) Hueber, A.J., et al. : Mast cells express IL-17A in rheumatoid arthritis synovium. J Immunol 184 : 3336-3340, 2010. – reference: 48) Lin, A.M., et al. : Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis. J Immunol 187 : 490-500, 2011. – reference: 16) Kotake, S., et al. : IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J Clin Invest 103 : 1345-1352, 1999. – reference: 22) Volpe, E., et al. : A critical function for transforming growth factor-beta, interleukin 23 and proinflammatory cytokines in driving and modulating human T(H)-17 responses. Nat Immunol 9 : 650-657, 2008. – reference: 5) Guedez, Y.B., et al. : Genetic ablation of interferon-gamma up-regulates interleukin-1beta expression and enables the elicitation of collagen-induced arthritis in a nonsusceptible mouse strain. Arthritis Rheum 44 : 2413-2424, 2001. – reference: 38) Zheng, Y., et al. : Interleukin-22, a T(H)17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Nature 445 : 648-651, 2007. – reference: 10) Willenborg, D.O., et al. : IFN-gamma plays a critical down-regulatory role in the induction and effector phase of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis. J Immunol 157 : 3223-3227, 1996. – reference: 14) Cua, D.J., et al. : Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature 421 : 744-748, 2003. – reference: 33) Griffiths, C.E., et al. : Comparison of ustekinumab and etanercept for moderate-to-severe psoriasis. N Engl J Med 362 : 118-128, 2010. – reference: 2) Smolen, J.S., et al. : The role of T-lymphocytes and cytokines in rheumatoid arthritis. Scand J Rheumatol 25 : 1-4, 1996. – reference: 1) Mosmann, T.R., et al. : Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins. J Immunol 136 : 2348-2357, 1986. – reference: 39) Papp, K.A., et al. : Brodalumab, an anti-interleukin-17-receptor antibody for psoriasis. N Engl J Med 366 : 1181-1189, 2012. – reference: 49) Sandborn, W.J., et al. : Ustekinumab induction and maintenance therapy in refractory Crohn's disease. N Engl J Med 367 : 1519-1528, 2012. – reference: 20) Wilson, N.J., et al. : Development, cytokine profile and function of human interleukin 17-producing helper T cells. Nat Immunol 8 : 950-957, 2007. – reference: 28) Miossec, P., et al. : Interleukin-17 and type 17 helper T cells. N Engl J Med 361 : 888-898, 2009. – reference: 35) Johnson-Huang, L.M., et al. : Effective narrow-band UVB radiation therapy suppresses the IL-23/IL-17 axis in normalized psoriasis plaques. J Invest Dermatol 130 : 2654-2663, 2010. – reference: 24) Ivanov, I.I., et al. : The orphan nuclear receptor RORγt directs the differentiation program of proinflammatory IL-17+ T helper cells. Cell 126 : 1121-1133, 2006. – reference: 7) Ferber, I.A., et al. : Mice with a disrupted IFN-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J Immunol 156 : 5-7, 1996. – reference: 37) Chan, J.R., et al. : IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis. J Exp Med 203 : 2577-2587, 2006. – reference: 18) Mangan, P.R., et al. : Transforming growth factor-β induces development of the Th17 lineage. Nature 441 : 231-234, 2006. – reference: 8) Krakowski, M., Owens, T. : Interferon-gamma confers resistance to experimental allergic encephalomyelitis. Eur J Immunol 26 : 1641-1646, 1996. – reference: 23) McGeachy, M.J., et al. : TGF-beta and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain T(H)-17 cell-mediated pathology. Nat Immunol 8 : 1390-1397, 2007. – reference: 26) Veldhoen, M., et al. : The aryl hydrocarbon receptor links Th17-cell-mediated autoimmunity to environmental toxins. Nature 453 : 106-109, 2008. – reference: 15) Aggarwal, S., et al. : Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J Biol Chem 278 : 1910-1914, 2003. – reference: 27) Infante-Duarte, C., et al. : Microbial lipopeptides induce the production of IL-17 in Th cells. J Immunol 165 : 6107-6115, 2000. – reference: 42) Huh, J.R., et al. : Digoxin and its derivatives suppress Th17 cell differentiation by antagonizing RORgammat activity. Nature 472 : 486-490, 2011. – reference: 40) Leonardi, C., et al. : Anti-interleukin-17 monoclonal antibody ixekizumab in chronic plaque psoriasis. N Engl J Med 366 : 1190-1199, 2012. – reference: 25) Kimura, A., et al. : Aryl hydrocarbon receptor regulates Stat1 activation and participates in the development of Th17 cells. Proc Natl Acad Sci USA 105 : 9721-9726, 2008. – reference: 41) Solt, L.A., et al. : Suppression of Th17 differentiation and autoimmunity by a synthetic ROR ligand. Nature 472 : 491-494, 2011. – reference: 32) Genovese, M.C., et al. : LY2439821, a humanized anti-interleukin-17 monoclonal antibody, in the treatment of patients with rheumatoid arthritis : A phase I randomized, double-blind, placebo-controlled, proof-of-concept study. Arthritis Rheum 62 : 929-939, 2010. – reference: 36) Zaba, L.C., et al. : Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses. J Exp Med 204 : 3183-3194, 2007. – reference: 3) Manoury-Schwartz, B., et al. : High susceptibility to collagen-induced arthritis in mice lacking IFN-γ receptors. J Immunol 158 : 5501-5506, 1997. – reference: 30) Huang, W., et al. : Requirement of interleukin-17A for systemic anti-Candida albicans host defense in mice. J Infect Dis 190 : 624-631, 2004. |
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| Title | 治療標的としてのIL-23/IL-17連関 |
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| ispartofPNX | 日本臨床免疫学会会誌, 2013, Vol.36(4), pp.203-208 |
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